Hepatitis A is a highly contagious liver infection caused by the hepatitis A virus (HAV). Hepatitis A is an enterovirus transmitted by the orofecal route, such as contaminated food. It causes an acute form of hepatitis (inflammation of the liver), does not have a chronic stage, and will not cause any permanent damage to the liver. The patient’s immune system makes antibodies against Hepatitis A that confer immunity against future infection. A vaccine is available that will prevent infection from hepatitis A for life. Hepatitis A virus is one of six currently identified strains of viral hepatitis — the others are B, C, D, E and G. The strains differ in severity and in the way they spread.
The diagnosis is made by the detection of antibodies directed at the virus by the person infected (Serum IgM anti-HAV).
· There is no specific treatment for Hepatitis A. Sufferers are advised to rest, avoid fatty foods and alcohol (these may be poorly tolerated for some additional months during the recovery phase and cause minor relapses), eat a well-balanced diet, stay hydrated. The doctor may give some medicine for the symptoms.
· Immune globulin is a preparation of antibodies that can be given before exposure for short-term protection against hepatitis A and for persons who have already been exposed to hepatitis A virus. Immune globulin must be given within 2 weeks after exposure to hepatitis A virus for maximum protection.
· Alternative medicine:
1. In Europe, the herb milk thistle (Silybum marianum) has been used to treat jaundice and other liver disorders. Today, scientific studies have confirmed that the chief constituent of milk thistle, silymarin, may aid in healing and rebuilding the liver. Silymarin seems to stimulate the production of antioxidant enzymes that help the liver neutralize toxins. It also seems to increase the production of new liver cells and may even improve the severe scarring of cirrhosis.
2. In Indonesia we use Temulawak (Curcuma xanthorrhiza Roxb) as medicinal herb for hepatitis. It has bioactive compounds such as curcumin and desmethoxycurcumin with similar effect as silymarin.
Immune Response against Virus infection
Immunity to viral infection is caused by a variety of specific and nonspecific mechanisms. The activation of different immune functions and the duration and magnitude of the immune response depend on how the virus interacts with host cells (on whether it is a cytolytic, steady-state, latent, and/or integrated infection) and on how the virus spreads (by local, primary hematogenous, secondary hematogenous, and/or nervous system spread). Therefore, viral antigens may be present in different parts of the body depending on the route of spread and phase of infection.
Humoral Immunity: Virus and/or virus-infected cells can stimulate B lymphocytes to produce antibody (specific for viral antigens) Antibody neutralization is most effective when virus is present in large fluid spaces (e.g., serum) or on moist surfaces (e.g., the gastrointestinal and respiratory tracts). IgG, IgM, and IgA have all been shown to exert antiviral activity. Antibody can neutralize virus by: 1) blocking virus-host cell interactions or 2) recognizing viral antigens on virus-infected cells which can lead to antibody-dependent cytotoxic cells (ADCC) or complement-mediated lysis. IgG antibodies are responsible for most antiviral activity in serum, while IgA is the most important antibody when viruses infect mucosal surfaces.
Cell-Mediated Immunity: The term cell-mediated immunity refers to (1) the recognition and/or killing of virus and virus-infected cells by leukocytes and (2) the production of different soluble factors (cytokines) by these cells when stimulated by virus or virus-infected cells. Cytotoxic T lymphocytes, natural killer (NK) cells and antiviral macrophages can recognize and kill virus-infected cells. Helper T cells can recognize virus-infected cells and produce a number of important cytokines. Cytokines produced by monocytes (monokines), T cells, and NK cells (lymphokines) play important roles in regulating immune functions and developing antiviral immune functions.
Immune Response against bacterial infection
Numerous physical and chemical attributes of the host protect against bacterial infection. These defenses include the antibacterial factors in secretions covering mucosal surfaces and rapid rate of replacement of skin and mucosal epithelial cells. Once the surface of the body is penetrated, bacteria encounter an environment virtually devoid of free iron needed for growth, which requires many of them to scavenge for this essential element. Bacteria invading tissues encounter phagocytic cells that recognize them as foreign, and through a complex signaling mechanism involving interleukins, eicosanoids, and complement, mediate an inflammatory response in which many lymphoid cells participate. Antibody-mediated immunity (AMI) is probably most useful as an immune defense because of its ability to neutralize or destroy extracellular pathogens and to prevent occurrence of reinfection. Antibodies exist free in body fluids, e.g. serum, and membrane bound to B lymphocytes. Their function when membrane bound is to capture antigen for which they have specificity, after which the B lymphocytes will take the antigen into its cytoplasm for further processing. Free antibodies have the following functions:
Agglutination of particulate matter, including bacteria and viruses. IgM is particularly suitable for this, as it is able to change its shape from a star form to a form resembling a crab.
Opsonization i.e. coating of bacteria for which the antibody’s Fab region has specificity (especially IgG). This facilitates subsequent phagocytosis by cells possessing an Fc receptor, e.g. neutrophil polymorphonuclear leucocytes (“polymorphs”).
Neutralization of toxins released by bacteria e.g. tetanus toxin is neutralized when specific IgG antibody binds, thus preventing the toxin binding to motor end plates and causing persistent stimulation, manifest as sustained muscular contraction which is the hallmark of tetanic spasms. This applies particularly to IgG.
Immobilization of bacteria. Antibodies against bacterial ciliae or flagellae will hinder their movement and ability to escape the attentions of phagocytic cells. Again, only Fab is involved.
Complement activation (classical pathway) especially by the Fc region of IgM and IgG, leads eventually to death of bacteria by the terminal complement
Mucosal protection. This is provided mainly by IgA, and to a lesser degree, IgG. IgA acts chiefly by inhibiting pathogens from gaining attachment to mucosal surfaces. This is a Fab function.
Expulsion as a consequence of Mast cell degranulation. As a consequence of antigen e.g. parasitic worms, binding to specific IgE attached to mast cells by their receptor for IgE Fc, there is release of mediators from the mast cell. This leads to contraction of smooth muscle, which can result in diarrhoea, and expulsion of parasites.